Paraquat is widely used as an herbicide. The plants are destroyed when the leaf surfaces are exposed to paraquat and the herbicide is inactivated by absorption onto clay minerals. The paraquat toxicity in human has been well documented, the pulmonary tissue being the main target for paraquat toxicity. Toxicity in man occurs mainly after drinking solutions of these compounds or after inhalation of dust. Death mainly occurs after 2 to 5 days with pulmonary edema and congestion with hyaline membrane formation. Some animal species become hyperexcitable after doses and have convulsions after lethal doses. In view of the acute toxicity of this drug, attempts are being made in several laboratories to gain an insight into the mode of toxicity of this compound on the lung. The only information that is presently available is that paraquat appears to be transported by an energy dependent process and stored within the lung. The stored paraquat in lung tissue appears to not be metabolized and slowly excreted as such in urine, and thus accounts for all the toxic effects observed in the lungs. Various attempts are being made to understand the types of lung cells involved in the paraquat toxicity. The cells of the lung which has the highest capacity to take up and bind paraquet would be the likely target for paraquet toxicity. Since paraquat produces pulmonary edema and since cyclic AMP has been known to be involved in movement of ions across various membranes, we have studied the effect of paraquet on the levels of cyclic AMP in the lung.